Wound healing in the skin requires migration and hyperproliferation of keratinocytes. Integrin α3β1, among other members of the integrin family, mediates the attachment of basal epidermal keratinocytes to the basement membrane, so its role in adult skin and wound healing is of interest. Complicating such studies, however, are α3-integrin-null mice, which die during the neonatal period. Controversially, integrin α3β1 has also been independently reported to promote and inhibit keratinocyte migration in vitro. Arnoud Sonnenberg and colleagues (p. 278) now generate epidermis-specific α3-integrin-knockout mice to investigate the function of integrin α3β1 in wound re-epithelialisation. These mice are viable, but display local inflammation, hair loss, basement-membrane duplication and microblistering at the dermal-epidermal junction; hemidesmosome assembly and keratinocyte differentiation are not impaired. In the absence of integrin α3β1 there is no change in keratinocyte proliferation, the distribution of other integrins and the deposition of basement-membrane proteins in the wound bed, but wound healing is faster, suggesting accelerated keratinocyte migration. Supporting in vitro evidence shows that α3-integrin-deficient keratinocytes migrate with increased velocity and persistence. The authors' results support a role for α3β1 integrin in inhibiting the directional migration of keratinocytes in vitro and wound re-epithelialisation in vivo.
Integrin α3β1 runs interference
Integrin α3β1 runs interference. J Cell Sci 15 January 2009; 122 (2): e205. doi:
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